Transcript Document
PANCREATITIS
ACUTE PANCREATITIS
Pathophys- insult leads to leakage of pancreatic
enzymes into pancreatic and peripancreatic tissue
leading to acute inflammatory reaction
ACUTE PANCREATITIS
Etiologies
Idiopathic
Gallstones (or other
obstructive lesions)
EtOH
Trauma
Steroids
Mumps (& other viruses:
CMV, EBV)
Autoimmune (SLE,
polyarteritis nodosa)
Scorpion sting
Hyper Ca, TG
ERCP (5-10% of pts
undergoing procedure)
Drugs (thiazides,
sulfonamides, ACE-I,
NSAIDS, azathioprine)
EtOH and gallstones
account for 60-70%
of cases
ETIOLOGY
90% of cases due to alcohol or gallstones
1. Gallstone induced pancreatitis:
women have higher incidence of gallstone induced disease than men
men have a higher risk of disease with gallstones
theories: reflux vs direct obstruction
2. Alcohol induced pancreatitis:
10% of chronic alcoholics
theory: increase in secretions with concomitant increase in sphincter
resistance
Drugs
TRIVIA
What is the name of the scorpion that causes
pancreatitis?
Tityus Trinitatis
(Found in Central/
South America and
the Caribbean)
SIGNS & SYMPTOMS
Severe epigastric abdominal pain - abrupt onset (may
radiate to back)
Nausea & Vomiting
Weakness
Tachycardia
+/- Fever; +/- Hypotension or shock
Grey Turner sign - flank discoloration due to retroperitoneal
bleed in pt. with pancreatic necrosis (rare)
Cullen’s sign - periumbilical discoloration (rare)
Grey Turner sign
Cullen’s sign
DIFFERENTIAL
Not all inclusive, but may include:
Biliary
disease
Intestinal obstruction
Mesenteric Ischemia
MI (inferior)
AAA
Distal aortic dissection
PUD
EVALUATION
amylase…Nonspecific !!!
Amylase levels > 3x normal very suggestive of pancreatitis
May be normal in chronic pancreatitis!!!
Enzyme level severity
False (-): acute on chronic (EtOH); HyperTG
False (+): renal failure, other abdominal or salivary gland
process, acidemia
lipase
More sensitive & specific than amylase
EVALUATION
Other inflammatory markers will be elevated
ALT > 3x normal gallstone pancreatitis
CRP, IL-6, IL-8 (studies hoping to use these markers to aid in
detecting severity of disease)
(96% specific, but only 48% sensitive)
Depending on severity may see:
Ca
WBC
BUN
Hct
glucose
RADIOGRAPHIC EVALUATION
AXR - “sentinel loop” or small bowel ileus
US or CT may show enlarged pancreas with stranding,
abscess, fluid collections, hemorrhage, necrosis or
pseudocyst
MRI/MRCP newest “fad”
Decreased nephrotoxicity from gadolinium
Better visualization of fluid collections
MRCP allows visualization of bile ducts for stones
Does not allow stone extraction or stent insertion
Endoscopic US (even newer but used less)
Useful in obese patients
CT SCAN OF ACUTE PANCREATITIS
CT shows
significant
swelling
and
inflammation
of the
pancreas
GALL STONE PANCREATITIS BY ERCP
ACUTE PANCREATITIS
Morbidity and mortality highest if necrosis
present (especially if necroctic area infected)
Dual
phase CT scan useful for initial eval to look for
necrosis
However,
necrosis may not be present for 48-72 hours
PROGNOSIS
Many different scoring systems
Ranson (most popular & always taught in med-school)
No association found with score, and mortality or length of
hospitalization
APACHE II
CT severity Index
Recent studies show this to be most predictive of adverse outcomes
CT score > 5 associated with 15x mortality rate
Problem is 1 CT study showing this was conducted 72 hours after
admission (Ranson/Apache are 24 & 48 hours)
Imrie Score
Atlanta Classification used to help compare various
scores (clinical research trials)
RANSON CRITERIA
Admission
Age > 55
WBC > 16,000
Glucose > 200
LDH > 350
AST > 250
During first 48 hours
5% mortality risk with <2 signs
15-20% mortality risk with 3-4 signs
40% mortality risk with 5-6 signs
99% mortality risk with >7 signs
Hematocrit drop > 10%
Serum calcium < 8
Base deficit > 4.0
Increase in BUN > 5
Fluid sequestration > 6L
Arterial PO2 < 60
CT SEVERITY INDEX
CT Grade
A is normal (0 points)
B is edematous pancreas (1
point)
C is B plus extrapancreatic
changes (2 points)
D is severe extrapancreatic
changes plus one fluid
collection (3 points)
E is multiple or extensive fluid
collections (4 points)
Necrosis score
None (0 points)
< 1/3 (2 points)
> 1/3, < 1/2 (4 points)
> 1/2 (6 points)
TOTAL SCORE =
CT grade + Necrosis
0-1 = 0% mortality
2-3 = 3% mortality
4-6 = 6% mortality
7-10 = 17% mortality
DETERMINANT-BASED CLASSIFICATION OF ACUTE
PANCREATITIS SEVERITY
AN INTERNATIONAL MULTIDISCIPLINARY
CONSULTATION
THERAPY
Remove offending agent (if possible)
Supportive !!!
#1- NPO (until pain free)
NG
suction for patients with ileus or emesis
TPN may be needed
#2- Aggressive volume repletion with IVF
Keep
an eye on fluid balance/sequestration and
electrolyte disturbances
THERAPY CONTINUED
#3- Narcotic analgesics usually necessary for pain
relief…textbooks say Meperidine…
NO conclusive evidence that morphine has
deleterious effect on sphincter of Oddi pressure
#4- Urgent ERCP and biliary sphincterotomy within
72 hours improves outcome of severe gallstone
pancreatitis
Reduced biliary sepsis, not actual improvement of
pancreatic inflammation
#5- Don’t forget PPI to prevent stress ulcer
COMPLICATIONS
Necrotizing pancreatitis
Significantly increases morbidity & mortality
Usually found on CT with IV contrast
Pseudocysts
Suggested by persistent pain or continued high amylase
levels (may be present for 4-6 wks afterward)
Cyst may become infected, rupture, hemorrhage or
obstruct adjacent structures
Asymptomatic, non-enlarging pseudocysts can be watched and
followed with imaging
Symptomatic, rapidly enlarging or complicated pseudocysts need
to be decompressed
COMPLICATIONS CONTINUED #2
Infection
Many areas for concern: abscess, pancreatic necrosis,
infected pseudocyst, cholangitis, and aspiration pneumonia
-> SEPSIS may occur
If concerned, obtain cultures and start broad-spectrum
antimicrobials (appropriate for bowel flora)
In the absence of fever or other clinical evidence for
infection, prophylactic antibiotics is not indicated
Renal failure
Severe intravascular volume depletion or acute tubular
necrosis may lead to ARF
COMPLICATIONS CONTINUED #3
Pulmonary
Atelectasis,
pleural effusion, pneumonia and ARDS
can develop in severe cases
Other
Metabolic
disturbances
hypocalcemia,
GI
hypomagnesemia, hyperglycemia
bleeds
Stress
Fistula
gastritis
formation
PROGNOSIS
85-90% mild, self-limited
Usually
resolves in 3-7 days
10-15% severe requiring ICU admission
Mortality
may approach 50% in severe cases